The bacterial effector HopM1 suppresses PAMP‐triggered oxidative burst and stomatal immunity

Abstract

Summary Successful pathogens counter immunity at multiple levels, mostly through the action of effectors. Pseudomonas syringae secretes c. 30 effectors, some of which have been shown to inhibit plant immunity triggered upon perception of conserved pathogen‐associated molecular patterns (PAMPs). One of these is HopM1, which impairs late immune responses through targeting the vesicle trafficking‐related AtMIN7 for degradation. Here, we report that in planta expressed HopM1 suppresses two early PAMP‐triggered responses, the oxidative burst and stomatal immunity, both of which seem to require proteasomal function but are independent of AtMIN7. Notably, a 14‐3‐3 protein, GRF8/AtMIN10, was found previously to be a target of HopM1 in vivo, and expression of HopM1 mimics the effect of chemically and genetically disrupting 14‐3‐3 function. Our data further show that the function of 14‐3‐3 proteins is required for PAMP‐triggered oxidative burst and stomatal immunity, and chemical‐mediated disruption of the 14‐3‐3 interactions with their client proteins restores virulence of a HopM1‐deficient P. syringae mutant, providing a link between HopM1 and the involvement of 14‐3‐3 proteins in plant immunity. Taken together, these results unveil the impact of HopM1 on the PAMP‐triggered oxidative burst and stomatal immunity in an AtMIN7‐independent manner, most likely acting at the function of (a) 14‐3‐3 protein(s).

The Proteasome Acts as a Hub for Plant Immunity and Is Targeted by Pseudomonas Type III Effectors

“…This could result in an inefficient degradation of other substrates and could explain why AtMIN7 is removed by the proteasome while overall proteasome activity is reduced. Besides its function to destabilize AtMIN7 and thereby interfere with vesicle trafficking, HopM1 also has an AtMIN7-independent function: it is able to suppress ROS production and stomatal closure during plant immunity (Lozano-Durán et al, 2014). The increased protein levels of FLS2 observed in HopM1-expressing cells supports the hypothesis that impaired proteasome activity may interfere with the proper recycling of the receptor, thereby dampening the PTI response.…”

Phosphorylation of the Plant Immune Regulator RPM1-INTERACTING PROTEIN4 Enhances Plant Plasma Membrane H+-ATPase Activity and Inhibits Flagellin-Triggered Immune Responses in Arabidopsis

“…Furthermore, some P. syringe effectors enhance growth on the surface of plant leaves (Lee et al, 2012). The P. syringae effector HopM1 can suppress stomatal immunity (Lozano-Durán et al, 2014). Recently, the AvrB, HopX1, and HopZ1a effectors have been demonstrated to activate JA signaling (Cui et al, 2010;Jiang et al, 2013;GimenezIbanez et al, 2014).…”

“…Pto uses coronatine, a jasmonic acid (JA) mimic, to induce stomatal opening (Melotto et al, 2006). The Pto effector HopM1 can also suppress stomatal immunity (Lozano-Durán et al, 2014). RIN4, AHA1/2, and multiple innate immune receptors are expressed in guard cells (Ueno et al, 2005;Liu et al, 2009b).…”

HLB1 Is a Tetratricopeptide Repeat Domain-Containing Protein That Operates at the Intersection of the Exocytic and Endocytic Pathways at the TGN/EE in Arabidopsis

“…In addition, protein traffic through endomembranes is pivotal for specifying how plants respond and adapt to a range of biotic and abiotic stresses (Chen et al, 2008;Lozano-Durán et al, 2014;Garcia de la Garma et al, 2015). The endomembrane system is highly dynamic and consists of a network of functionally interconnected organelles beginning with the endoplasmic reticulum (ER) where proteins are synthesized and then trafficked to the plasma membrane (PM) and vacuole after processing and sorting in the Golgi apparatus and post-Golgi organelles (Richter et al, 2009;Brandizzi and Barlowe, 2013).…”